Vitamin D from coming from tissues (vs blood) was speculated to be 50% in 2014, and by 2017 was speculated to be 90%

Note: Good results from a blood test (> 40 ng) does not mean that a good amount of Vitamin D actually gets to cells

A Vitamin D test in cells rather than blood was feasible (2017 personal communication)

Commercially available 2019However test results would vary in each tissue due to multiple genes

Good clues that Vitamin D is being restricted from getting to the cells
1) A vitamin D-related health problem runs in the family especially if it is one of 51+ diseases related to Vitamin D Receptor2) Slightly increasing Vitamin D show benefits (even if conventional Vitamin D test shows an increase)
3) Vitamin D Receptor test (<$30) scores are difficult to understand in 2016
easier to understand the VDR 23andMe test results analyzed by FoundMyFitness in 2018
4) Back Pain probably want at least 2 clues before taking adding vitamin D, Omega-3, Magnesium, Resveratrol, etcThe founder of VitaminDWiki took action with clues #3&4

Our sample consisted of 1,829 participants randomly selected from the Sister Study, a cohort of women who had a sister with breast cancer but had never had breast cancer themselves. 19,741 SNPs were associated with 25(OH)D (p < 0.05). We re-assessed these hits in an independent sample of 1,534 participants who later developed breast cancer. After pooling, 32 SNPs had genome-wide significant associations (p < 5 × 10-8).

These were located in or near GC, the vitamin D binding protein, or CYP2R1, a cytochrome P450 enzyme that hydroxylates vitamin D to form 25(OH)D. The top hit was rs4588, a missense GC polymorphism associated with a 3.5 ng/mL decrease in 25(OH)D per copy of the minor allele (95% confidence interval [CI]: -4.1, -3.0; p = 4.5 × 10-38). The strongest SNP near CYP2R1 was rs12794714, a synonymous variant (p = 3.8 × 10-12; β = 1.8 ng/mL decrease in 25(OH)D per minor allele [CI: -2.2, -1.3]). Serum 25(OH)D concentrations from samples collected from some participants 3-10 years after baseline (811 cases, 780 non-cases) were also strongly associated with both loci. These findings augment our understanding of genetic influences on 25(OH)D and the possible role of vitamin D binding proteins and cytochrome P450 enzymes in determining measured levels. These results may help to identify individuals genetically predisposed to vitamin D insufficiency.

PMID: 29545823 PMCID: PMC5838824 DOI: 10.3389/fgene.2018.00067

Created by admin.
Last Modification: Sunday March 18, 2018 11:27:53 GMT-0000 by admin.
(Version 6)